Thoracic Anesthesia Flashcards
Describe the hemodynamic changes seen in pulmonary hypertension
- fixed afterload d/t increased pressure in the pulmonary artery
- preload-dependent BUT TOO MUCH RV volume overload shifts the interventricular septum to the LV –> lower systemic CO
- high demand conditions may be detrimental: severe exertion, pregnancy (labor)
*PA pressure = CO (right-side) x PVR + LA pressure
*Cor Pulmonale - RV failure d/t high PAP
*pulmonary capillaries: greatest drop in pressure and increase in resistance
List drugs that are considered pulmonary vasodilators
- calcium channel blockers: nifedipine, diltiazem, amlodipine - block contraction of pulmonary artery smooth muscle
- prostacyclin analog: epoprosterenol
- inhaled NO
- PDE-5 inhibitors: sildenafil
- Nitrates: NTG, sodium nitroprusside
Differentiate nitroglycerin from nitroprusside
Nitroglycerin
- venous > arterial dilation
- decrease preload
- coronary vasodilator: preferred if with concurrent ischemic episodes
- WOF: methemoglobinemia
Sodium Nitroprusside
- equal venous & arterial dilation
- decrease afterload
- reported coronary steal
- WOF: methemoglobinemia, cyanide toxicity
Conduct of anesthesia for pulmonary hypertension
Inducting agent: propofol, etomidate (ketamine - controversial increase in PVR)
Avoid histamine-releasing NMB
Avoid high concentrations of volatile agents, and use of N2O
Avoid excessive hypotension, RV afterload to ensure perfusion
Adequate pain control and normothermia
What should be avoided triggers of increased PVR?
hypoxia
hypercarbia
acidosis
Ventilation strategies for pulmonary hypertension
a) ‘luxury’ oxygenation FiO2 0.6-1.0
b) low TV ~6ml/kg IBW
c) moderate hyperventilation PaCO2 30-35 mmHg
d) avoid metabolic acidosis pH > 7.4
e) PEEP 5-10 cmH2O
*maximize FiO2 first before increasing PEEP to minimize the hemodynamic effect of high PEEP on preload
Vasoactive use in pulmonary hypertension
Vasopressin - choice
Vasopressin, Epinephrine, Dopamine (no/minimal effect on PVR)
Dobutamine, milrinone (lowers PVR): do not use alone because of systemic vasodilation
NE
phenylephrine, ephedrine - AVOIDED
*Maintain systemic pressure above pulmonary pressure to preserve coronary blood flow
Expected ABG finding during an asthma attack
respiratory alkalosis
hypoxemia
hypocarbia
*CO2 retention is a late finding of severe and prolonged airway obstruction i.e. status asthmaticus
Earliest benefit of smoking cessation
12 hours - lower carboxyhemoglobin levels, rightward shift of the hemoglobin dissociation curve
*6-8 weeks - optimal for elective surgery
Anesthetic considerations for asthmatics/COPD (GA/RA)
1) block airway reflexes esp. during airway manipulation
2) relax airway smooth muscles
3) prevent release of biochemical mediators
Propofol or ketamine
Sevoflurane > desflurane > isoflurane (least pungent)
Avoid histamine-releasing NMB e.g. atracurium, mivacurium
LMA over intubation if possible
Neuraxial block: avoid block above T10 - may reduce effective coughing
Ventilation strategies for asthma/COPD
- pressure control over volume control
- increase expiratory time: I/E ratio
- permissive hypoventilation/hypercapnia
- PIP < 50 cmH2O
- Plateau pressure < 30 cmH2O
What is auto-PEEP?
Auto-PEEP or intrinsic PEEP aka breath stacking
- inadequate exhalation –> gas trapping –> increasing intrathoracic pressure –> (a) barotrauma, volutrauma, dyssynchrony
(b) lower VR –> CV collapse
- in mechanically ventilated patients w/ asthma/COPD
Most common cause of intraoperative bronchospasm
Inadequate depth of anesthesia
How to proceed in case of intraoperative wheezing/bronchospasm?
Increase FiO2 while looking for causes
- check PIP, plateau pressure (possible differentials)
- check ETT & circuit
- auscultate chest
- stop surgical stimulation: traction on the mesentery, GIT –> vagal reflex
- LAST: B-agonist 8-10 puffs via ETT
How to differentiate between changes in inspiratory and plateau pressures?
HIGH PIP, N plateau: resistance - kinked ETT/circuit, mucus plug
HIGH PIP & plateau: compliance - pneumonia, pulmonary edema
